Evidence map›Paper›PMID 36284177›Full record

ArticleScientific reports2022

The synergy of β amyloid 1-42 and oxidative stress in the development of Alzheimer's disease-like neurodegeneration of hippocampal cells.

Gohar Karapetyan, Katarine Fereshetyan, Hayk Harutyunyan, Konstantin Yenkoyan

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  8. Intranasal AβJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  9. Review
  10. Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  11. Mechanistic Insights into the Neuroprotective Potential ofPharmaceuticals (Basel, Switzerland) · 2025
    Article
  12. Article
  13. Article
  14. Comparative Study of Injected Alzheimer's Disease Models in Rats: Insights from Experimental Research.Pathophysiology : the official journal of the International Society for Pathophysiology · 2024
    Article
  15. Article
  16. Review
  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Gohar KarapetyanNeuroscience Laboratory, Cobrain Center, Yerevan State Medical University named after M. Heratsi, 2 Koryun Str., 0025, Yerevan, Armenia.
Katarine FereshetyanNeuroscience Laboratory, Cobrain Center, Yerevan State Medical University named after M. Heratsi, 2 Koryun Str., 0025, Yerevan, Armenia.
Hayk HarutyunyanNeuroscience Laboratory, Cobrain Center, Yerevan State Medical University named after M. Heratsi, 2 Koryun Str., 0025, Yerevan, Armenia.
Konstantin YenkoyanNeuroscience Laboratory, Cobrain Center, Yerevan State Medical University named after M. Heratsi, 2 Koryun Str., 0025, Yerevan, Armenia. konstantin.yenkoyan@meduni.am.
Yerevan State Medical University · AM

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a type of dementia that affects memory, thinking and behavior. Symptoms eventually become severe enough to interfere with daily tasks. Understanding the etiology and pathogenesis of AD is necessary for the development of strategies for AD prevention and/or treatment, and modeling of this pathology is an important step in achieving this goal. β-amyloid peptide (Aβ) injection is a widely used approach for modeling AD. Nevertheless, it has been reported that the model constructed by injection of Aβ in combination with a prooxidant cocktail (ferrous sulfate, Aβ, and buthionine sulfoximine (BSO) (FAB)) best reflects the natural development of this disease. The relationship between oxidative stress and Aβ deposition and their respective roles in Aβ-induced pathology in different animal models of AD have been thoroughly investigated. In the current paper, we compared the effects of Aβ 1-42 alone with that of Aβ-associated oxidative stress induced by the FAB cocktail on the neurodegeneration of hippocampal cells in vitro. We constructed a FAB-induced AD model using rat primary hippocampal cells and analyzed the contribution of each compound. The study mainly focused on the prooxidant aspects of AD pathogenesis. Moreover, cellular bioenergetics was assessed and routine metabolic tests were performed to determine the usefulness of this model. The data clearly show that aggregated Aβ1-42 alone is significantly less toxic to hippocampal cells. Aggregated Aβ damages neurons, and glial cells proliferate to remove Aβ from the hippocampus. External prooxidant agents (Fe

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAntioxidantsButhionine SulfoximineDisease Models, AnimalHippocampusOxidative StressPeptide FragmentsRatsReactive Oxygen SpeciesAmyloid beta-PeptidesAntioxidantsButhionine SulfoximinePeptide FragmentsReactive Oxygen Species

Identifiers

PMID36284177
PMCPMC9596457
OpenAlexW4307208474

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.